Exposure to copper and copper-based nanoparticles induces hepatopancreatic mitochondrial dysfunction by triggering mtROS mediated apoptosis and mitophagy in Eriocheir sinensis

• Published in: The Science of the total environment 2024-11, p.177576, Article 177576
• Main Authors: Guo, Xinping, Shen, Minghao, Jiang, Su, Xing, Xiumei, Zhang, Cong, Yin, Shaowu, Zhang, Kai
• Format: Article
• Language: English
• Subjects: Apoptosis; Cu-NPs; CuSO4; Mitophagy; Oxidative stress
• ISSN: 0048-9697; 1879-1026; 1879-1026
• DOI: 10.1016/j.scitotenv.2024.177576

Copper (Cu) is an important metal pollutant commonly found in aquatic environment owing to its inherent bioaccumulation and biomagnification potentials and long-term persistence in environmental compartments. The application of novel fabricated copper nanoparticles (Cu-NPs) has led to cytotoxicity in aquatic animals. However, the differences in underlying toxicity mechanisms between Cu-NPs and waterborne Cu (such as CuSO4) remain unelucidated. Herein, the mechanisms underlying the CuSO4/Cu-NPs-mediated perturbation of the hepatopancreatic mitochondrial function at different concentrations were investigated and compared. After exposing Eriocheir sinensis to 0 (control), 5, 50, and 500 μg/L CuSO4 and 10 μg/L Cu-NPs for 21 days, hepatopancreases were retrieved. The results revealed that Cu-NPs or CuSO4 (50 and 500 μg/L) induced ultrastructural damage following a time-dose effect, as indicated by swelling and degeneration of the lumen of hepatic tubules. Excess CuSO4 or Cu-NPs exposure decreased the antioxidative capacity and led to the over-accumulation of mitochondrial ROS. Moreover, the mitochondrial membrane potential (ΔΨm) was reduced and apoptosis induced. Additionally, both CuSO4 and Cu-NPs increased the numbers of mitophagosomes and the mRNA and protein levels of LC3B, and triggered mitophagy through PRKN-independent pathway; however, mostly the BNIP3L/Beclin1 pathway was involved in excess CuSO4-induced mitophagy. Altogether, this study provides a basis for exploring Cu-mediated potential mitochondrial autophagy activation mechanisms and their effects on environmental toxicity. [Display omitted] •Both Cu-NPs or CuSO4 can induced ultrastructural damage and over-accumulation of mitochondrial ROS in E. sinensis.•Cu treatment reduced mitochondrial membrane potential and triggered hepatopancreatic apoptosis.•Both Cu-NPs or CuSO4 caused mitophagy through PRKN-independent pathway.•BNIP3L/Beclin1 pathway was involved in excess CuSO4-induced mitophagy.